Manfredini Fabio, Giusti Fabiola, Beani Laura, Dallai Romano
Dipartimento di Biologia Evolutiva, University of Siena, Siena 53100, Italy.
J Morphol. 2007 Jul;268(7):588-601. doi: 10.1002/jmor.10540.
To successfully complete its endoparasitic development, the strepsipteran Xenos vesparum needs to elude the defense mechanisms of its host, the wasp Polistes dominulus. SEM and TEM observations after artificial infections allow us to outline the steps of this intimate host-parasite association. Triungulins, the mobile 1st instar larvae of this parasite, are able to "softly" overcome structural barriers of the larval wasp (cuticle and epidermis) without any traumatic reaction at the entry site, to reach the hemocoel where they settle. The parasite molts 48 h later to a 2nd instar larva, which moves away from the 1st instar exuvium, molts twice more without ecdysis (a feature unique to Strepsiptera) and pupates, if male, or develops into a neotenic female. Host encapsulation involves the abandoned 1st larval exuvium, but not the living parasite. In contrast to the usual process of encapsulation, it occurs only 48 h after host invasion or later, and without any melanization. In further experiments, first, we verified Xenos vesparum's ability to reinfect an already parasitized wasp larva. Second, 2nd instar larvae implanted in a new host did not evoke any response by hemocytes. Third, we tested the efficiency of host defense mechanisms by implanting nylon filaments in control larval wasps, excluding any effect due the dynamic behavior of a living parasite; within a few minutes, we observed the beginning of a typical melanotic encapsulation plus an initial melanization in the wound site. We conclude that the immune response of the wasp is manipulated by the parasite, which is able to delay and redirect encapsulation towards a pseudo-target, the exuvia of triungulins, and to elude hemocyte attack through an active suppression of the immune defense and/or a passive avoidance of encapsulation by peculiar surface chemical properties.
为了成功完成其体内寄生发育，捻翅目昆虫黄尾小蜂需要避开其宿主——黄胸胡蜂的防御机制。人工感染后的扫描电子显微镜（SEM）和透射电子显微镜（TEM）观察使我们能够勾勒出这种亲密的宿主-寄生虫关联的步骤。该寄生虫的活动一龄幼虫——三爪蚴，能够“轻柔地”克服黄蜂幼虫的结构屏障（角质层和表皮），在进入部位没有任何创伤反应，从而到达它们定居的血腔。寄生虫在48小时后蜕变为二龄幼虫，它会离开一龄幼虫的蜕皮，再蜕两次皮（这是捻翅目独有的特征）且不蜕皮，然后化蛹（如果是雄性），或者发育成幼态雌性。宿主包囊化涉及被遗弃的一龄幼虫蜕皮，但不涉及活的寄生虫。与通常的包囊化过程不同，它仅在宿主被入侵48小时后或更晚才发生，并且没有任何黑化现象。在进一步的实验中，首先，我们验证了黄尾小蜂再次感染已被寄生的黄蜂幼虫的能力。其次，植入新宿主的二龄幼虫没有引起血细胞的任何反应。第三，我们通过在对照黄蜂幼虫中植入尼龙丝来测试宿主防御机制的效率，排除了活寄生虫动态行为产生的任何影响；在几分钟内，我们观察到典型的黑化包囊化开始以及伤口部位的初始黑化。我们得出结论，黄蜂的免疫反应受到寄生虫的操纵，寄生虫能够延迟包囊化并将其重新导向一个假目标——三爪蚴的蜕皮，并通过主动抑制免疫防御和/或凭借特殊的表面化学性质被动避免包囊化来躲避血细胞的攻击。
